Effect of 5-caffeoylquinic acid on the NF-κB signaling pathway, peroxisome proliferator-activated receptor gamma 2, and macrophage infiltration in high-fat diet-fed Sprague-Dawley rat adipose tissue.

Obesity, considered as a consequence of overnutrition, sustains a low-degree inflammatory state and results in insulin-resistance and type 2 diabetes. Here, we investigated the anti-inflammatory effects of 5-caffeoylquinic acid (5-CQA) in high-fat diet-induced obese rats. Serum interleukin (IL)-6, monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-alpha (TNF-α), total cholesterol (TC), triglyceride (TG), and free fatty acid (FFA) levels were determined. Expression of genes related to TG metabolism, macrophage biomarkers, and inflammation was assessed by real-time PCR. Protein expression of NF-κB, PPARγ2, and phosphorylated IκBα was evaluated by western blotting, and the histology of adipose tissue was examined. Supplementation of the rat diet with 5-CQA reduced obesity development, macrophage infiltration, and steatosis. Additionally, 5-CQA decreased the expression of NF-κB and downstream inflammatory cytokines, but increased the expression of PPARγ2, in a dose-dependent manner. Thus, 5-CQA improved obesity and obesity-related metabolic disturbances via PPARγ2 and the NF-κB signaling pathway.

Chlorogenic Acid Maintains Glucose Homeostasis through Modulating the Expression of SGLT-1, GLUT-2, and PLG in Different Intestinal Segments of Sprague-Dawley Rats Fed a High-Fat Diet.

OBJECTIVE: To reveal the effects and related mechanisms of chlorogenic acid (CGA) on intestinal glucose homeostasis. METHODS: Forty male Sprague-Dawley rats were randomly and equally divided into four groups: normal chow (NC), high-fat diet (HFD), HFD with low-dose CGA (20 mg/kg, HFD-LC), and HFD with high-dose CGA (90 mg/kg, HFD-HC). The oral glucose tolerance test was performed, and fast serum insulin (FSI) was detected using an enzyme-linked immunosorbent assay. The mRNA expression levels of glucose transporters (Sglt-1 and Glut-2) and proglucagon (Plg) in different intestinal segments (the duodenum, jejunum, ileum, and colon) were analyzed using quantitative real-time polymerase chain reaction. SGLT-1 protein and the morphology of epithelial cells in the duodenum and jejunum was localized by using immunofluorescence. RESULTS: At both doses, CGA ameliorated the HFD-induced body weight gain, maintained FSI, and increased postprandial 30-min glucagon-like peptide 1 secretion. High-dose CGA inhibited the HFD-induced elevation in Sglt-1 expression. Both CGA doses normalized the HFD-induced downregulation of Glut-2 and elevated the expression of Plg in all four intestinal segments. CONCLUSION: An HFD can cause a glucose metabolism disorder in the rat intestine and affect body glucose homeostasis. CGA can modify intestinal glucose metabolism by regulating the expression of intestinal glucose transporters and Plg, thereby controlling the levels of blood glucose and insulin to maintain glucose homeostasis.